Exogenic alterations of the skin

5  Non-tumorous skin diseases

5.18  Exogenic alterations of the skin

5.18.1  Scar

5.18.2  Cauterisatio

Clinical signs:

  • limited to directly affected skin
  • if the damage is slight, then erythema, burning
  • acids: coagulation necrosis
  • lye: colliquation necrosis


Cauterisatio, lysol (lye)
Cauterizatio, CLINIC (678)

Cauterisatio, persteril (peracetic acid)
Cauterizatio, CLINIC (679)

5.18.3  Combustio (burns)

Clinical signs:

  • 1st grade: erythema
  • 2nd grade: bullae
  • 3rd grade: necrosis
  • higher grades heal with mutilating, keloid scars


Scalding, keloid scars:
Combustio, CLINIC (682)

Combustio bullosa:
Combustio bullosa, CLINIC (2839)

Combustio bullosa, CLINIC (2840)

Further examples of thermal injury:


Arteficial changes of the cells (elongated cells or cell nuclei), necrosis, inflammation, reparation.


Acute deep burn (death in fire), no signs of reparation:
Thermal burn, HE 40x (5280)

Healing burn caused by CO2 laser:
Laser burn, HE 20x (4746)

Skin defect and scar after burn:
Scar after burn, HE 40x (4769)

5.18.4  Congelatio (frostbite)

Clinical signs:

  • acute frostbite:
    • 1st grade, erythema;
    • 2nd grade, bullae;
    • 3rd grade, necroses
  • chronic cold causes chillblains (perniones), red or purple macules (nose, ears, fingers, thighs)
  • hypersensitivity to cold can be caused by other diseases (vascular disorders, cryoglobulinemia)


Frostbite, ear, 2nd grade: erythema, edema, bulla:
Congelatio, CLINIC (691)

Pernio, CLINIC (5822)

Pernio, CLINIC (5823)

Further examples of pernio:


Acute frostbire, 3rd grade: necroses, vital reaction (inflammation). After cryalisation is the tissue necrotic.


Pernio, HE 20x (4935)

Pernio, HE 20x (5390)

Pernio, HE 20x (5391)

Cryalisation of the basalioma, followed by resection:
Cryocoagulated bazalioma, HE 40x (6071)

Epidermal necrosis caused by liquid nitrogen (medical treatment):
Liquid nitrogen necrosis, HE 20x (13877)

5.18.5  Livedo e calore, erythema ab igne


Caused by prolonged exposure to heat.

Clinical signs:

  • persistent reticular erythematous lesion

5.18.6  Dermatitis artefacta


Skin lesion, caused by the patient itself.

Clinical signs:

  • location: anywhere, ofter whithin reach of the patient
  • atypical blisters, ulcers, nodules etc.


Artificial dermatitis, abdomen (rectangular shape of the lesion)
Dermatitis artefacta, CLINIC (705)  Arteficial dermatitis, caused by spray

Clinical signs:

Arteficial lesion, caused by young girl on purpose by cooling her skin by closely positioned spray.


Superficial areas of the epidermis are necrotic, homogenous, eosinophilic, partially detached.


Arteficial dermatitis, spray:
Arteficial dermatitis (close spray), HE 60x (12970)

5.18.7  Haematoma

Clinical signs:

Posttraumatic extravasation of blood into soft tissues.


Bleeding within the tissue (dermis, fat).

5.18.8  Radiodermatitis


Caused by damage of the skin by irradiation, usually during actinotherapy of malignant tumors.


Further examples of radiodermatitis are in the chapter in:  Radiodermatitis acute

Clinical signs:

  • extent according to irradiated area of the skin
  • 1st grade: erythema, burning, tranient hair loss, decrease of secretion of sebaceous glands, residual pigmentations
  • 2nd grade: blisters, madidation, crusts, permanent loss of hair, damage of sebaceous and sweat glands
  • 3rd grade: acute actinic ulceration, impaired healing


Radiodermatitis acuta
Radiodermatitis acuta, CLINIC (907)

Betatron reaction:
Betatron reaction, HE 40x (1963)


Vesicles, ulcerations, erosions.  Radiodermatitis, chronic

Clinical signs:

  • develops years after irradiation, follows radiodermatitis of 2nd and 3rd grade, but can develop after low dose, cummulative irradiations
  • atrophy, sclerosis, loss of adnexa
  • teleangiectasia, changes of pigmentation, keratoses
  • these changes are called poikiloderma
  • chronic ulceration, carcinoma


Epidermis is atrophic, dermis with sclerosis and hyalinisation, hair adnexa are lost, eccrine glands are atrophic. Dilated blood vessels and scattered fibroblasts with large, polymorphous nuclei. Focal pigment incontinence is sometimes present. Epidermis may be dysplastic.

5.18.9  Phototoxic and photoallergic reactions


Phototoxic dermatitis is caused by contact or ingestion of some photosensitizing substance. Phytophotodermatitis affects anyone, who gets in contact with some plants containing furocoumarins and later gets exposed to sunlight (dermatitis striata praetensis of Hebra).

Photoallergic dermatitis appears after exposure to some photosensitizing agent (usually drugs) applied on the skin and following exposure to sunlight. The reaction develops in senzitized persons by delayed hypersensibility reaction.

Acute solar dermatitis is caused by severe UV irradiation of a sensitive skin. In phototoxic and protoallergic reactions some photosensibilizing agens is effective as well (some drugs, desinfecting agents, various plants etc.)

Polymorphous solar eruption affects insolation areas, more often women; prutitus, papules, vesicles.

Dermatitis vernalis aurium Dermatosis of the auricles. Affects young people at spring, caused by sunshine combined with cold.

Actinic reticuloid form of a chronic actinic reaction.

Solar urticaria immediate urticarial response to sunshine

Hydroa vacciniforme rare disease of children, characterized by hemorrhagic blisters and necroses

Clinical signs:

  • 1st grade: erythema, burning sensation
  • 2nd grade: blisters
  • 3rd grade: necrosis (rare)
  • late stage: pigmentations, peeling


Phototoxic dermatitis: dyskeratosis, necroses (in less severe forms of individual keratinocytes only). Alteration of the basal layer.

Photoallergic dermatitis is characterized by spongiosis, dyskeratosis, perivascular lymphocytic infiltrate with variable admixture of neutrophils.

Polymorphous light eruption: variable picture, some spongiosis, usually scattered necrotic or dyskeratotic keratinocytes, variable vacuolar degeneration; dermal edema; perivascular lymphocytic infiltrate; sometimes extravasation of erythrocytes. Sometimes subepidermal or intraepidermal vesicles.

5.18.10  Berloque dermatitis

Clinical signs:

  • phototoxic reaction (oil of bergamot)
  • this oils is a part of some perfumes; the most common location is therefore the neck
  • the skin gets reddish at first, later brown pigmentation develops
  • pigmentation is long lasting or permanent

5.18.11  Syndrome Favre-Racouchot

Clinical signs:

  • location: face, esp. around the eyes (sun exposed areas)
  • multiple open dilated comedons similar to those in acne vulgaris
  • affects elder people
  • prominent solar elastosis in underlying skin


Dilated follicular ostia, cystic comedones, atrophy of the epidermis, solar elastosis, sometimes papillomatosis

5.18.12  Actinic damage of the skin


UV radiation:

200 — (UVC) — 280 — (UVB) — 320 — (UVA) — 400

UVA causes mainly pigmentation, UVB has inflammatory effect followed by pigmentation. UV irradiation of the skin can be used for therapy. Sensitivity of the skin to sunshine is highly individual. Main changes to the skin caused by UV irradiation are:

caused by stimulation of melanocytes
Acute solar dermatitis
after intesive and/or prolonged exposure to sun
Polymorphous light eruption
seen at spring at sensitive people  — papular eruption after short exposure
Chronic actinic dermatitis and actinic reticuloid
widespread pruritic eczematoid reaction, especially in elderly men
Phototoxic and photoallergic dermatitis
combination of sun exposure and some substances, esp. drugs
Increased photosensitivity
in some diseases, eg. porphyria cutanea tarda
Degeneration of the connective tissue of the corium
after long lasting sun exposure (esp. in elderly) homogenous, gray-blue, orcein positive material is accumulated within the papillary corium
Solar keratosis
dysplastic changes of the epidermis; in situ squamous cell carcinoma
Squamous cell carcinoma
higher frequency on sun-damaged skin
occurs especially on sun-damaged skin
Malignant melanoma
higher frequency on sun-damaged skin

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